Potassium-dependent prolonged field bursts in the dentate gyrus: effects of extracellular calcium and amino acid receptor antagonists.
Potassium-dependent prolonged field bursts in the dentate gyrus: effects of extracellular calcium and amino acid receptor antagonists.
复制标题
齿状回钾依赖性延长场爆发：细胞外钙和氨基酸受体拮抗剂的作用。
DOI：
10.1016/0306-4522(94)90055-8
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发表时间：
1994
期刊：
影响因子：
3.3
通讯作者：
Dudek,FE
中科院分区：
文献类型：
--
作者：
Patrylo,PR;Schweitzer,JS;Dudek,FE
The dentate gyrus in rat hippocampal slices produces spontaneous, prolonged bursts of population spikes (i.e. prolonged field bursts) when [Ca2+]0is lowered (0-0.5 mM) and [K+]0is concurrently elevated (9–11 mM). In this investigation we examined whether the dentate gyrus could also generate spontaneous field bursts in relatively “normal” (i.e. nominal 1.3 mM) or only moderately decreased [Ca2+]0(i.e. nominal 0.9 mM). In 1.3 mM [Ca2+]0, no prolonged field bursts occurred spontaneously in the dentate gyrus when [K+]0was raised as high as 12 mM. Prolonged field bursts were generated, however, when [K+]0was further increased to 13–15 mM. Similar bursts could be generated at [K+]0within the “physiological ceiling level” observedin vivoduring seizure activity (i.e. 11–12 mM) if: (i) the bath [Ca2+] was reduced to 0.9 mM; or (ii) the GABA type A-receptor antagonist bicuculline was added in the presence of “normal” (1.3 mM) [Ca2+]0. Adding both theN-methyl-d-aspartate and nonN-methyl-d-aspartate receptor antagonists, (±)-2-amino-5-phosphonopentanoic acid (50–100 μM) and 6,7-dinitroquinoxaline-2,3-dione (50–100 μM), respectively, did not block the occurrence of the field bursts. The bursts generated in 1.3 mM [Ca2+]0, 12 mM [K+]0, bicuculline, (±)-2-amino-5-phosphonopen-tanoic acid and 6,7-dinitroquinoxaline-2,3-dione could, however, be reversibly depressed or blocked if [Ca2+]0was raised to 2.0 mM.These data suggest that: (i) the dentate gyrus (like CA1) can produce prolonged field bursts in “normal” [Ca2+]0when [K+]0is elevated, although the [K+]0threshold is higher; (ii) the dentate gyrus can generate prolonged field bursts in response to [K+]0elevations within the physiological ceiling, provided [Ca2+]0is moderately lowered (i.e. 0.9 mM) or GABA type A-transmission is blocked; and (iii) antagonists of excitatory amino acid-mediated neurotransmission do not block the prolonged field bursts produced under any of these conditions.
